Pain Management Flashcards

1
Q

Types of Pain

A

NOCICEPTIVE PAIN

Nociceptive pain is pain in response to a noxious stimulus at nociceptors that are located in different tissues. This system is a key physiologic function that prevents further tissue damage due to the body’s autonomic withdrawal reflex.

Nociceptive pain is typically classified as either somatic (arising from skin, bone, joints, muscle or connective tissue) or visceral (arising from internal organs such as the large intestine or the pancreas).

INFLAMMATORY PAIN

When tissue damage occurs despite the nociceptive defense system, inflammatory pain ensues. The body now changes focus from protecting against painful stimuli to protecting the injured tissue. The inflammatory response contributes to pain hypersensitivity that serves to prevent contact or movement of the injured part until healing is complete, thus reducing further damage.

NEUROPATHIC PAIN

Neuropathic pain results from damage to or dysfunction of the peripheral or central nervous system, rather than stimulation of pain receptors. Patients tend to describe neuropathic pain with words like burning, tingling, numbness, shooting, stabbing, or electric-like feelings. Although neuropathic pain may respond well to opioids, adjuvant analgesics (tricyclic antidepressants, anticonvulsants, etc) are often required in combination with opioids to achieve adequate relief.

FUNCTIONAL PAIN

Functional pain is pain sensitivity due to an abnormal processing or function of the central nervous system in response to normal stimuli. Several conditions considered to have this abnormal sensitivity include fibromyalgia and irritable bowel syndrome.

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2
Q

NOT RECOMMENDED ANALGESICS FOR ROUTINE DOSING

A

MEPERIDINE

Meperidine is poorly absorbed orally and has a short half-life of approximately 3 hours. Its principal metabolite, normeperidine, has no analgesic properties, has a half-life of about 15 - 20 hours, is renally excreted, and produces significant adverse effects when it accumulates, such as tremulousness, dysphoria, myoclonus, and seizures. Consequently, meperidine is not recommended for routine dosing.

MIXED AGONIST-ANTAGONISTS

Mixed agonist-antagonists are not recommended as routine analgesics, as their dosing is limited by a ceiling effect. Doses cannot be greatly increased to treat increasing pain without greatly increasing incidence or severity of side effects.

Additionally, pentazocine, nalbuphine, and butorphanol are associated with psychotomimetic adverse effects.

Mixed opioid agonist-antagonists should not be used in a patient already taking a pure agonist opioid (codeine, hydrocodone, hydromorphone, methadone, morphine, oxycodone): Competition for the opioid receptors may cause a withdrawal reaction.

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3
Q

Combination Therapy

A

COMBINATION THERAPY

The combination of opioid and nonopioid analgesics often results in analgesia superior to that produced by either agent alone. This facilitates the use of lower doses and a more favorable side-effect profile, and, when needed, this approach is encouraged.

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4
Q

Managing Opioid Adverse Effects

A

The most common adverse effects reported with the use of opioid analgesics are nausea, vomiting, sedation, itching and constipation.

Urticaria, pruritus:

In some patients, opioids produce urticaria or pruritus. These effects are the result of mast cell destabilization by the opioid and subsequent histamine release. Usually the rash and pruritus can be managed by administration of hydroxyzine or diphenhydramine.

Constipation:

Constipation secondary to opioid administration is almost universal. It is primarily the result of opioid effects on the central nervous system, spinal cord, and myenteric plexus of gut that, in turn, reduce gut motor activity and increase stool transit time.

Tolerance to constipation may develop very slowly, if at all. As a general rule, a laxative should be prescribed when an opioid is started. For most patients, a stimulant laxative (eg, senna or bisacodyl) counteracts opioid-induced constipation. While stool softeners (eg, docusate) are not usually effective by themselves, combination stimulant/softeners (eg, senna + docusate) can be useful.

If constipation persists, some patients will benefit from the addition of an osmotic agent, such as magnesium hydroxide or lactulose.

Note: Bulk-forming agents (eg, psyllium) require substantial fluid intake and are not recommended for those with advanced disease and poor mobility.

Nausea/vomiting

Many patients starting opioids experience nausea with or without vomiting. It usually disappears as tolerance develops within a few days. It can be treated with hydroxyzine, metoclopramide or prochlorperazine.

Sedation

Opioid-induced sedation usually disappears over a few days as tolerance develops. Persistent opioid-induced sedation that limits activity can be ameliorated with amphetamine, methylphenidate or modafinil.

Respiratory depression

Many physicians have an exaggerated view of the risk of respiratory depression when using opioids to relieve pain. Pain is a potent stimulus to breathe, and pharmacologic tolerance to respiratory depression develops quickly.

If respirations are compromised, naloxone may be necessary.

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5
Q

ANALGESIC ADJUNCTIVE AGENTS (COANALGESICS)

A

Adjuvant analgesics are pharmacologic agents which are useful in the management of pain but that are not primarily classified as analgesics. They can be used as monotherapy or in combination with non-opioids and opioids. They include antidepressants, anticonvulsants, glucocorticoids, and other drugs.

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6
Q

Imipramine

A

TRICYCLIC ANTIDEPRESSANTS

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7
Q

Amitriptyline

A

TRICYCLIC ANTIDEPRESSANTS

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8
Q

Desipramine

A

TRICYCLIC ANTIDEPRESSANTS

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9
Q

Nortriptyline

A
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10
Q

ANTIDEPRESSANTS AND ANTICONVULSANTS

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ANTIDEPRESSANTS AND ANTICONVULSANTS

Antidepressants and anticonvulsants are the mainstay of treatment for a variety of neuropathic pain syndromes, even though many of them are not approved by the FDA for these indications.

ANTIDEPRESSANTS

Serotonin and norepinephrine mediate descending inhibition of ascending pain pathways in the brain and spinal cord.

Antidepressant agents that enhance both serotonergic and noradrenergic transmission, such as the tricyclic antidepressants (TCAs), and the serotonin and norepinephrine reuptake inhibitors (SNRIs), display significant analgesic effects.

Antidepressant agents that enhance only serotonergic transmission, such as the selective serotonin reuptake inhibitors (SSRIs) are less effective analgesics.

Tricyclic antidepressants (TCAs) can relieve many types of neuropathic pain, including diabetic neuropathy, postherpetic neuralgia, polyneuropathy, and nerve injury or infiltration with cancer. They are also effective in fibromyalgia pain.

TCAs commonly used as analgesics are desipramine, nortriptyline, amitriptyline and imipramine.

MECHANISM OF ACTION

TCAs cause analgesia by inhibiting norepinephrine and serotonin reuptake, thus enhancing the action of these neurotransmitters.

ADVERSE EFFECTS

The most common adverse effects of TCAs (constipation, dry mouth, blurred vision, cognitive changes, tachycardia, urinary hesitation) are associated with their anticholinergic activity. Other common adverse effects are sexual dysfunction, orthostatic hypotension, weight gain, and sedation.

In general, the secondary amines (e.g., desipramine, nortriptyline) exhibit fewer anticholinergic and sedative effects than do the tertiary amines (e.g., amitriptyline, imipramine); therefore, the secondary amines may be more desirable in the elderly population.

WARNINGS, PRECAUTIONS & CONTRAINDICATIONS

Tricyclic antidepressants should be administered cautiously in patients with angle-closure glaucoma, benign prostatic hypertrophy, urinary retention, constipation, cardiovascular disease, or impaired liver function. They should be avoided in patients with second- or third-degree heart block, arrhythmias, prolonged QT interval on the electrocardiogram, or severe liver disease and in patients who have had a recent acute myocardial infarction.

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11
Q

VENLAFAXINE AND DULOXETINE

A

SEROTONIN AND NOREPINEPHRINE REUPTAKE INHIBITORS (SNRIs)

VENLAFAXINE AND DULOXETINE

SNRIs selectively inhibit the reuptake of both serotonin and norepinephrine. The SNRIs differ from the TCAs in that they lack the potent antihistamine, α-adrenergic blocking, and anticholinergic effects of the TCAs.

Venlafaxine and duloxetine are effective for several types of neuropathic pain.

ADVERSE EFFECTS

Adverse effects of the SNRIs include nausea, sexual dysfunction, and somnolence. The adverse effect profile of the SNRIs is favorable relative to the TCAs.
SNRIs are better tolerated than the TCAs.

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12
Q

Gabapentin

A

ANTICONVULSANTS

Gabapentin is indicated for the management of postherpetic neuralgia.

MECHANISM OF ACTION

Gabapentin and pregabalin block voltage-gated calcium-channels. This leads to reduction of the influx of calcium into neurons which may decrease the release of glutamate, norepinephrine, and substance P.

ADVERSE EFFECTS

The main adverse effects of gabapentin and pregabalin are dizziness, somnolence, and peripheral edema.

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13
Q

Pregabalin

A

ANTICONVULSANTS

Pregabalin is approved for management of neuropathic pain associated with postherpetic neuralgia, diabetic neuropathy, and fibromyalgia.

MECHANISM OF ACTION

Gabapentin and pregabalin block voltage-gated calcium-channels. This leads to reduction of the influx of calcium into neurons which may decrease the release of glutamate, norepinephrine, and substance P.

ADVERSE EFFECTS

The main adverse effects of gabapentin and pregabalin are dizziness, somnolence, and peripheral edema.

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14
Q

Carbamazepine

A

ANTICONVULSANTS

Carbamazepine is the drug of choice for treatment of pain due to trigeminal neuralgia.

MECHANISM OF ACTION

Voltage-gated sodium channels in sensory neurons play a crucial role in neuropathic pain. The analgesic activity of carbamazepine is associated with blockade of voltage-gated sodium channels.

ADVERSE EFFECTS

Adverse effects of carbamazepine include drowsiness, dizziness, nausea and vomiting. Carbamazepine-induced leukopenia is not uncommon, but it is usually benign; aplastic anemia is a rare side effect.

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15
Q

Glucocorticoids

A

Glucocorticoids are commonly used in advanced illness. They may be useful for acute nerve compression, increased intracranial pressure, bone pain, visceral pain (obstruction and/or capsular distention), anorexia, nausea, and depressed mood.

Dexamethasone, with its long half-life and minimal mineralocorticoid effect, is the drug of choice.

Prednisone and methylprednisolone can also be used.

Glucocorticoids have several other indications. They can improve appetite, nausea, malaise, and overall quality of life.

Although the risk of adverse effects increases with both the dose and duration of therapy, long-term treatment with relatively low doses is generally well tolerated.

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16
Q

Hydroxyzine

A

Hydroxyzine may add to the analgesic effect of opioids in postoperative and cancer pain while reducing the incidence of nausea and vomiting.

17
Q

Clonidine

A

Clonidine. Available as oral and transdermal patch formulations. May improve pain and hyperalgesia in sympathetically maintained pain.

18
Q

Lidocaine

A

A lidocaine patch is approved for treatment of postherpetic neuralgia.

19
Q

Capsaicin

A

A capsaicin patch is approved for treatment of postherpetic neuralgia.

20
Q

Caffeine

A

Caffeine may enhance the analgesic effect of acetaminophen and NSAIDs.